Skip to main content
. Author manuscript; available in PMC: 2010 Mar 12.
Published in final edited form as: Auton Neurosci. 2008 Oct 31;146(1-2):3–7. doi: 10.1016/j.autneu.2008.09.005

Figure 4. Cardiovascular response to tyramine in rabbits with EAAG.

Figure 4

Rabbits were implanted with radiotelemetry catheters to allow continuous recording of arterial blood pressure and heart rate in the awake rabbit. Tyramine, an indirect sympathetic agonist, was infused intravenously over one minute (0.5mg/kg). A) Blood pressure and heart rate response to tyramine infusion. A rise in blood pressure (as seen in both control and EAAG rabbits) indicates intact postganglionic sympathetic nerve terminals. In the control rabbits, the rise in blood pressure leads to a baroreflex-mediated decrease in heart rate. In the EAAG rabbit, both the blood pressure and heart rate increase. This observation indicates failure of the baroreflex as well as direct activation of cardiac beta receptors via intact cardiac sympathetic terminals. B) A summary of the tyramine response in control rabbits (n=9), rabbits with chronic EAAG (n=13), and normal rabbits after treatment with the ganglionic blocker mecamylamine (3 mg/kg, n=3). In all rabbits, tyramine causes a rise in blood pressure (open bars). The magnitude of blood pressure increase is greater in EAAG and mecamylamine-treated rabbits, most likely due to failure of the sympathetic baroreflex to buffer the rise in blood pressure. In control rabbits, there is a marked baroreflex-mediated decrease in heart rate (shaded bar) while the EAAG and mecamylamine-treated rabbits show an increase in heart rate. This unique response to tyramine shows the similarity in autonomic physiology between EAAG and pharmacological blockade of ganglionic transmission.